Alzheimer's disease is characterized by the accumulation of a 39–43 amino acid peptide termed the beta-amyloid protein or Aβ, in a fibrillar form, existing as extracellular amyloid plaques and as amyloid within the walls of cerebral blood vessels. Fibrillar Aβ amyloid deposition in Alzheimer's disease is believed to be detrimental to the patient and eventually leads to toxicity and neuronal cell death, characteristic hallmarks of Alzheimer's disease. A variety of morphologically distinct types of Aβ-containing plaques have been described in the brains of Alzheimer's disease patients including diffuse plaques (which demonstrate Aβ immunoreactivity but do not stain for fibrillar amyloid using amyloid stains such as Congo red and Thioflavin S), neuritic plaques (which contain a central amyloid core which stains with Congo red and Thioflavin S, and which is surrounded by dystrophic neurites) and compact, burned-out or “amyloid star” plaques (which usually demonstrate a maltese-cross pattern when stained with Congo red and viewed under polarized light). Investigators have hypothesized that in Alzheimer's disease there is most likely a conversion from the diffuse plaque to the neuritic plaque to the compact, burned-out plaque. However, the mechanism of this conversion and the essential components involved have never been elucidated. In addition, the formation of compact plaques in vitro which demonstrate a maltese-cross pattern when stained with Congo red and viewed under polarized light has never been achieved.